Blood pressure and adrenal steroid biosynthesis in 7 patients with LREH was evaluated before and after treatment with aminoglutethimide (AG) (1 gm/day for 3 weeks). AG reduced BP in all patients, decreased the excretion of aldosterone 75%, and raised plasma renin activity into the normal range, but failed to decrease plasma concentrations of progesterone, 17-hydroxy progesterone, deoxycorticosterone, 18-hydroxydeoxycorticosterone, 11-desoxycortisol, or cortisol, or the urinary excretion of 16-beta-OH-dehydroepiandrosterone, 17-hydroxy or 17-ketosteroids. Secretion rates for 16-beta-OH DHEA were not changed by AG. The observation that chronic administration of aminoglutethimide lowered blood pressure in these patients and elevated their plasma renin activity to the normal range without decreasing production of the adrenal steroids, deoxycorticosterone, 18-hydroxydeoxycorticosterone and 16-beta-OH dehydroepiandrosterone, makes it unlikely that the steroids are responsible either for the suppressed renin or the elevated blood pressure in patients with low renin essential hypertension.